The tillering phenotype of the rice plastid terminal oxidase (PTOX) loss-of-function mutant is associated with strigolactone deficiency
The tillering phenotype of the rice plastid terminal oxidase (PTOX) loss-of-function mutant is associated with strigolactone deficiency
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DOI：
10.1111/nph.12630
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发表时间：
2014-04-01
期刊：
影响因子：
9.4
通讯作者：
Terauchi, Ryohei
中科院分区：
文献类型：
--
作者：
Tamiru, Muluneh;Abe, Akira;Terauchi, Ryohei
质体末端氧化酶（PTOX）在八氢番茄红素去饱和和叶绿体功能中的重要性已经通过PTOX缺陷突变体，特别是在拟南芥中得到证实。然而，关于它在单子叶植物中的作用的研究还很缺乏。在这里，我们报告克隆和表征的水稻利用生态型靶向诱导水稻PTOX 1基因的局部损伤（EcoTILLING）和TILLING作为正向遗传工具，我们鉴定了以过度分蘖为特征的EMS突变体的致病突变，与PTOX 1基因相对应的半矮秆和叶斑。ptox 1突变体的矮化表型与已知独脚金内酯（SL）相关的水稻突变体的表型相似，并且这两种表型性状都可以通过应用合成的SL GR 24来挽救。PTOX 1突变体积累八氢番茄红素在白色叶扇区与相应的β-胡萝卜素缺乏，与PTOX 1在促进八氢番茄红素去饱和酶活性的预期功能一致。在根分泌物中也没有类胡萝卜素衍生的SL ent-2 '-epi-5-deoxystrigol的积累。在突变体中检测到生长素的浓度升高，支持以前的观察，SL与生长素的相互作用是很重要的芽分支control.Our研究结果表明，PTOX 1是所需的类胡萝卜素和SL的合成导致SL-缺乏的表型在水稻。
The significance of plastid terminal oxidase (PTOX) in phytoene desaturation and chloroplast function has been demonstrated using PTOX-deficient mutants, particularly in Arabidopsis. However, studies on its role in monocots are lacking. Here, we report cloning and characterization of the rice (Oryza sativa) PTOX1 gene.Using Ecotype Targeting Induced Local Lesions IN Genomes (EcoTILLING) and TILLING as forward genetic tools, we identified the causative mutation of an EMS mutant characterized by excessive tillering, semi-dwarfism and leaf variegation that corresponded to the PTOX1 gene.The tillering and semi-dwarf phenotypes of the ptox1 mutant are similar to phenotypes of known strigolactone (SL)-related rice mutants, and both phenotypic traits could be rescued by application of the synthetic SL GR24. The ptox1 mutant accumulated phytoene in white leaf sectors with a corresponding deficiency in beta-carotene, consistent with the expected function of PTOX1 in promoting phytoene desaturase activity. There was also no accumulation of the carotenoid-derived SL ent-2'-epi-5-deoxystrigol in root exudates. Elevated concentrations of auxin were detected in the mutant, supporting previous observations that SL interaction with auxin is important in shoot branching control.Our results demonstrate that PTOX1 is required for both carotenoid and SL synthesis resulting in SL-deficient phenotypes in rice.